原发性翼状胬肉是一种上皮下生长的非肿瘤性变性组织，其发病机制主要与紫外线照射有关，然而，原发性翼状胬肉的具体发病机制仍不明确。近年来，随着医学研究的不断深入，研究显示原发性翼状胬肉的发生发展与多种因素息息相关。病毒感染、氧化应激、炎症反应，抑癌基因失活、DNA 甲基化等因素已被证实与翼状胬肉发病机制有关。此外，凋亡和增殖蛋白的失衡、细胞外基质调节剂和上皮-间充质细胞转化等因素也都在原发性翼状胬肉的发病过程中扮演着重要的角色。这些均可能导致细胞生长和分裂的异常，进而诱发翼状胬肉的形成。然而，各个因素之间的相互作用以及它们在发病过程中的具体作用机制仍有待进一步研究。该文中笔者就当前原发性翼状胬肉的发病机制进行评述，深入探究原发性翼状胬肉的发病机制及不同相关因素在原发性翼状胬肉发病过程中的相互作用。了解不同因素在发病过程中的作用，可以为临床提供更加精准、有效的预防和治疗策略提供依据，为患者带来更好的治疗效果和更高生活质量。

Primary pterygium is a non-neoplastic degenerative tissue that grows subepithelially, and its pathogenesis is mainly related to ultraviolet exposure, however, the full mechanism of primary pterygium remains unclear. In recent years, with the development of medical research, it is found that the occurrence and development of primary pterygium are closely related to a variety of factors. Viral infection, oxidative stress, inflammatory response, inactivation of tumor suppressor genes, DNA methylation and other factors have been shown to be involved in the pathogenesis of pterygium. In addition, imbalances of apoptosis and proliferative proteins, extracellular matrix regulators, and epithelial-mesenchymal cell transformation also play important roles in the pathogenesis of primary pterygium. These can lead to abnormal cell growth and division, which in turn induces the formation of pterygium. However, the interaction between these factors and their specific mechanisms of action in the pathogenesis process still need to be further studied. In this article it reviews the current pathogenesis of primary pterygium, and deeply explores the pathogenesis of primary pterygium and the interaction of different related factors in the pathogenesis of primary pterygium. By understanding the role of different factors in the pathogenesis process, we can provide more precise and effective prevention and treatment strategies for clinical practice, and better treatment outcomes and quality of life for patients.

目的：探究T盒转录因子2(T-box transcription factor 2,TBX2)在葡萄膜黑色素瘤(uveal melanoma,UVM)中的表达水平、生存预后、免疫浸润相关性。方法：首先通过TIMER2.0数据库分析正常组织和肿瘤组织中TBX2表达和临床特征，从UCSC Xena数据库下载泛癌的生存数据，使用Cox比例风险模型和Kaplan-Meier曲线分析评估TBX2对预后的预测价值。然后使用cBioPortal数据库分析人源TBX2突变前后生存改变，通过BloodSpot和TIMER2.0数据库探究TBX2与癌症免疫浸润之间的相关性。癌症单细胞状态图谱和基因集变异分析(gene set variation analysis,GSVA)探究其表达与分子机制的相关性。结果： 15种肿瘤类型的TBX2 mRNA表达水平显著改变，TBX2是肾上腺皮质癌(adrenocortical carcinoma,ACC)、肾乳头状细胞癌(kidney renal papillary cell carcinoma,KIRP)、UVM典型的生存预后标志物。其突变与生存状态无明显相关性，在UVM中T淋巴细胞浸润水平提高导致不良预后风险升高。此外，在UVM中TBX2通路富集至ATP结合盒(ATP-binding cassette transporter,ABC)转运蛋白、DNA修复和损伤。结论：TBX2在UVM的生存和免疫浸润中起着关键作用，将来可能作为一种UVM预后及免疫治疗效果的预测因子。

Objective: To investigate the expression level of T-box transcription factor 2(TBX2) in uveal melanoma (UVM), the correlation between survival prognosis and immune infiltration. Methods: The expression and clinical features of TBX2in normal and tumorwere analyzed by TIMER2.0 database. The survival data of pancarcinoma were downloaded from UCSC Xena database, and the prognotic value of TBX2 was evaluated using Cox proportional risk model and Kaplan-Meier curve analysis. Then cBioPortal database was used to analyze the changes before and after TBX2 mutation survivalin human, and BloodSpot and TIMER2.0 databases were used to explore the correlation between TBX2 and cancer immune infiltration. Cancer single cell status mapping and gene set variation analysis (GSVA) were used to explore the correlation between its expression and molecular mechanisms. Results: The mRNA expression levels of TBX2 were significantly changed in 15 tumor types. TBX2 is adrenocortical carcinoma (ACC) and kidney renal papillary cell carcinoma (Kidney renal papillary cell carcinoma). KIRP and UVM are typical prognostic markers of survival. The mutation had no significant correlation with survival status, and increased T cell infiltration level in UVM led to increased risk of poor prognosis. In addition, the TBX2 pathway is enriched to the ATP-binding cassette transporter (ABC) transporters, DNA repair, and damage in UVM. Conclusion: TBX2 plays a key role in survival and immune invasion of uveal melanoma.and may be used as a predictor of UVM prognosis and immunotherapy effect in the

future.

原发性获得性鼻泪管阻塞(primary acquired nasolacrimal duct obstruction，PANDO)是泪道阻塞性疾病中最常见的一类，好发于中老年女性，是眼科临床上的常见病、多发病，常继发急性或慢性泪囊炎的症状和体征，严重影响患者的日常工作和生活。本文对近年来PANDO可能的发病机制相关的研究进展、亟待解决的问题及未来研究的热点方向作一综述，旨在进一步加深对泪道阻塞性疾病发生发展的认识。

Primary acquired nasolacrimal duct obstruction (PANDO), which mainly occurs in the middle-aged and elderly women, is the most common type of obstructive diseases of the lacrimal duct, and it is also a common and frequently-occurring disease in ophthalmology. It constantly occurs secondary to various symptoms and signs of acute or chronic dacryocystitis, which seriously affects the daily work and life of patients. This article summarizes the research progress on the possible pathogenesis of PANDO in recent years, the urgent problems to be solved

and the hot research directions in the future, aiming to further deepen the understanding of the occurrence and development of lacrimal obstructive diseases.

眼睑皮脂腺癌是起源于眼睑部位皮脂腺体的恶性上皮性肿瘤，易复发、转移，主要治疗方式仍以手术切除为主，但患者整体预后并不理想，早期正确诊断和靶向治疗是改善患者预后和改进治疗的关键。眼睑皮脂腺癌临床表现复杂，早期容易误诊或漏诊进而延误治疗，病理检查是其诊断的金标准。此外，目前关于眼睑皮脂腺癌发病机制未完全阐明，癌发生发展的分子生物学过程尚未明确。因此，多方面了解眼睑皮脂腺癌发病机制为靶向治疗提供理论基础是十分必要的。本文主要从眼睑皮脂腺癌发病机制包括遗传因素、表观遗传、外源病毒感染、免疫逃逸、端粒酶学说等方面对眼睑皮脂腺癌作一综述。

Eyelid sebaceous gland carcinoma is a malignant epithelial tumor originating from eyelid sebaceous glands, which is prone to relapse and metastasis. The treatment mainly depends on surgical excision, but the overall prognosis of patients is not ideal. Early diagnosis and targeted therapy are the keys to improve the prognosis of patients.Due to its complex clinical manifestations, early misdiagnosis or missed diagnosis is easy to delay treatment, and pathological examination is still the gold standard for its diagnosis. In addition, the pathogenesis of eyelid sebaceous gland carcinoma is still unclear, and the molecular biological process of the occurrence and development is less understood. Therefore, it is very necessary to understand the pathogenesis of eyelid sebaceous gland carcinoma in various aspects to provide a theoretical basis for targeted therapy. In this paper, the pathogenesis of eyelid sebaceous gland carcinoma was reviewed from the aspects of gene , epigenetic, viral infection, immune escape, , telomerase theory and so on.

干眼是以泪膜稳态丢失及伴随眼部不适症状为特征的最常见眼表疾病，泪膜不稳定、泪液高渗透性、眼表炎症及感觉神经异常为其主要病因。地夸磷索钠是一种P2Y2受体激动剂，能刺激黏蛋白及泪液分泌，其独特的作用机制为干眼的治疗开辟了新的方向，本文就地夸磷索钠近年的临床及基础研究进展作一综述。

Dry eye is one of the most common ocular surface diseases. It is characterized by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and tear hyperosmolarity, ocular surface inflammation, and neurosensory abnormalities play major etiological roles. Diquafosol tetrasodium is a purinergic P2Y2 receptor agonist that promotes mucin and aqueous tear secretion. The unique pharmacological mechanism of diquafosol tetrasodium opens up a new direction for the medical therapies of dry eye. This article reviews the clinical therapeutic effect and research progress of diquafosol tetrasodium for the past few years.

过敏性结膜炎经典的发病机制包括了IgE介导的I型超敏反应以及T淋巴细胞介导的IV型超敏反应，其中肥大细胞、肥大细胞脱颗粒释放的组胺、嗜酸性粒细胞等在过敏性结膜炎病理发展中发挥了重要作用。然而，临床发现针对上述机制的治疗药物临床疗效欠佳，有相当数量的过敏性结膜炎患者无法获得较好的生存质量，因此研究和阐明过敏性结膜炎的新机制，寻找新的治疗手段和药物靶点具有重要的临床意义。目前研究发现Th17细胞等多种炎性细胞和IL-17等细胞因子、过敏原介导神经调节机制、菌群失调机制、脂质介质作用方面可能与过敏性结膜炎发病相关，这对过敏性结膜炎新机制的研究有着重大的临床意义。本文将对过敏性结膜炎发病机制的新进展进行综述，以期为过敏性结膜炎的治疗提供新思路。

The classic pathogeneses of allergic conjunctivitis include type I hypersensitivity and type IV hypersensitivity, in which mast cells, eosinophils and some active substances such as histamine play important role. However, sincethe therapeutic drugs have not achieved satisfactory efficacy in clinical practices, a significant number of patients fail to achieve a good quality of life. The pathogenesis of allergic conjunctivitis remains to be further studied.Current studies have identified a variety of inflammatory cells such as Th17 cell and cytokines such as IL-17, the mechanisms of neuromodulation, flora dysregulation mechanisms, and lipid mediators that may be involved in the pathogenesis of allergic conjunctivitis, which has significant clinical implications for the study of mechanisms of allergic conjunctivitis. In this article, we will review the recent research progress of the pathogenesis of allergic conjunctivitis in order to provide new ideas for the treatment of allergic conjunctivitis.

睑板腺功能障碍(meibomian gland dysfunction，MGD)是一种慢性、弥漫性的睑板腺病变，通常以睑板腺终末导管的阻塞或分泌的睑脂数量或质量发生改变为特征，临床上可以引起泪膜异常、角膜上皮损害、眼部刺激等干眼表现。MGD病因复杂且受多种因素影响，因此MGD发病机制的研究对于指导临床工作至关重要。本文对研究MGD的动物模型进行了介绍，并根据一些基础研究对MGD相关的细胞及分子机制等方面进行综述。

Meibomian gland dysfunction (MGD) is a chronic and diffuse disease of the eyelid gland. It is usually characterized by obstruction of the terminal duct of the eyelid gland or changes in the quantity/quality of the eyelid fat secreted. It can clinically cause dry eye symptoms such as abnormal tear film, corneal epithelial damage and eye irritation. The etiology of MGD is complex and affected by a variety of factors. Therefore, the study on the pathogenesis of MGD is of great importance to guide clinical work. This article introduces the animal research model of MGD, and reviews the cellular and molecular mechanisms related to MGD based on some basic research.

在晶状体纤维细胞分化的终末阶段，细胞核、线粒体、内质网及高尔基体等膜性细胞器会发生程序性的降解，这对晶状体透明性的维持至关重要。然而，晶状体细胞器降解过程的机制尚不明确。研究晶状体细胞器的降解过程可为阐明白内障的发病机制提供理论依据，也有望为晶状体再生提供新的干预靶点。本文就晶状体细胞器降解过程及其机制进行综述。

During terminal differentiation of lens fiber cells, nuclei and other organelles experience programmed elimination.This process is essential for the maintenance of lens transparency. However, the mechanisms underlying lens organelle degradation remain unclear. Identification of the mechanisms can provide a theoretical basis for elucidating the pathogenesis of cataract and is expected to reveal new intervention targets for lens regeneration. In this review, we discuss potential mechanisms and the process of lens organelle degradation.